Inflammatory periodontal disease (periodontitis) is a widely prevalent oral disease. In its severe form, it is characterized by gradual resorption of the alveolar bone which retains and supports the teeth. The affected teeth become loose, and eventually are supported inadequately for retention in the mouth. Commonly, more than one tooth is affected simultaneously and it is not unusual for ten or twenty teeth to be lost during the same period.
Present therapy for periodontal disease involves surgical removal of healthy bone in an attempt to eliminate gingival pocket depth which retains all bacteria and thereby to slow progression of the disease. Chemical therapies, such as use of weak acids to wash the involved root surfaces, have not provided satisfactory results in severe forms of the disease. Previously, no one has suggested use of a polymer to treat periodontal disease.
The primary cause of periodontal disease is thought to be the presence of bacterial toxins in the diseased root which cause failure of gingival cells to maintain a topologically continuous, bacteria-tight seal around the tooth root. It is theorized that bacteria colonize exposed root surfaces, where they or their toxic products, or both, cause further detachment of gingiva and, in severe cases, resorption of proximal alevolar bone. Regular mechanical debridement leads to some improvement, supporting current thinking about the primary cause of the disease. However, attempts to maintain a bacteria-free environment have not been generally effective in cases within which bone loss has occurred and an open soft tissue cuff or pocket exists.
The present invention solves this problem by interposing between the diseased tooth root surface and the overlying gingiva a material which permits mammalian cells to attach biologically. By using a material which is also impermeable to the toxic products of bacteria which have colonized the root surface, biological reattachment of the gingiva and reapproximation of alveolar bone are encouraged.
Although some plastics support attachment and growth of mammalian fibroblastic and epithelial cells (which are the major living constituents of normal gingiva) in cell culture, certain of these, such as polystyrene, require toxic or cumbersome pre-treatments to enable the to do so, including acid washes or electron bombardment inside a glow discharge apparatus. Other plastics, such as methylmethacrylate, do not permit biological attachment of mammalian cells in vivo or in vitro. Still others, such as teflon, may permit biological attachment of mammalian cells in both animal and in culture, but are not useful as coatings because they are insoluble and cannot be cast as a film.
In the event of extensive tooth loss due to inflammatory periodontal disease or trauma, it is not possible to provide patients with fixed dentures because insufficient structural support remains in the mouth. Current therapy involving insertion of dental implants to which fixed dentures may be attached is unsatisfactory. The implants are unreliable and have high failure frequencies because of lack of gingival attachment to the implants and bacterial migration along the implants which lead to resorption of the alveolar bone which supports and retains them. The reasons for bone resorption around implants and around periodontally involved tooth roots are believed to be identical, namely, bacteria penetrate between the implant and the gingival soft tissue and secrete toxins promoting epithelial invagination and bone resorption. The process may be more severe in implants. Periodontally involved tooth roots usually have some degree of gingival attachment at the base of epithelial invagination to protect them from bacterial invasion, but, currently available implants are unable to form a bacteria-tight seal with the gingival tissue. Although the gingival tissue presses closely againt the implant, there is access for bacteria to enter and multiply. One reason these implants do not form protective seals is that their outer surfaces are made of materials unable to support biological attachment of mammalian cells.
Although a wide variety of materials are used, most implants involve porous outer layers to encourage fibrous ingrowth for mechanical support. Examples of such porous coatings are vitreous carbon (U.S. Pat. No. 3,971,134; 1976) and mixtures of polymethacrylate with grated anorganic bone (U.S. Pat. No. 3,609,867; 1971). U.S. Pat. No. 3,971,134 also discloses biologically inert polymers such as polymethylmethacrylate, polyethylene, and polytetrafluoroethylene as porous implant coatings. Finally, U.S. Pat. No. 3,906,550 (1975) discloses fiber metal implant coatings.
Other coatings include calcium compounds (U.S. Pat. No. 3,984,914; 1976) to promote formation of cemetoid-type structures around the implant and nonporous polymethylmethacrylate (U.S. Pat. No. 4,060,896; 1977). However, neither coating forms a bacteria-tight seal with alveolar bone. Methacrylate, in particular, is incapable of molecular attachment to tissue (Hammer, J. E. and O. M. Reed., J. Biomed. Mater. Res. Symposium 1972, 2 (pt 2), 297-310). Instead, the body forms fibrous capsules around the methacrylate. In general, the prior art teaches that nonporous implant coatings, e.g. methacrylate, would be less effective than porous coatings of the same composition because of inadequate mechanical support associated with nonporous coatings. In this way, the art teaches away from the present invention by disclosing the use of porous, biologically inert materials, such as methylmethacrylate, carbon, and the like.
The materials presently used as coatings in prosthetic devices, such as orthopedic and maxillofacial prostheses, also teach away from this invention. Typically, the coatings are porous and have the deficiencies described above. These materials also exhibit high creep or poor load distribution under stress, or both (U.S. Pat. No. 4,164,794; 1979). Non-porous bioglasses have been used in prosthetic devices to promote direct bone-to-implant bonding (Griss, P. et al., J. Biomed. Mater. Res. 1976, 10, 511-518 and Blencke, B. A. et al., J.Biomed.Mater.Res. 1978, 12, 307-316). However, bioglasses do not form bonds with soft tissues (Clark, et al., J.Biomed.Mater.Res. 1976, 10, 161-174). None of these disclosures teach the use of nonporous, polymeric coatings in applications involving soft tissue (e.g., gingiva.) All involve hard tissue (e.g., fractured bone.)